Bees are important insect pollinators in both agricultural and natural settings who may encounter toxicants while foraging on plants growing in contaminated soils. How these chemicals affect the bee microbiome, which confers many health benefits to the host, is an important but understudied aspect of pollinator health. Through a combination of 16S rRNA gene sequencing, LC-MS metabolomics, ICP-OES spectroscopy, quantitative PCR, culturing, microbiome manipulation, and whole organism exposure studies, I attempt to establish the effects that toxicants have on social bees and their associated microbes.

The microbiome of animals has been shown to reduce metalloid toxicity, so I exposed microbiome-inoculated or uninoculated bumble bees to 0.75 mg/L selenate and found that inoculated bees survive longer when compared to uninoculated bees. I also showed that selenate exposure altered the composition of the bumble bee microbiome and that the growth of two major gut symbionts – Snodgrassella alvi and Lactobacillus bombicola – was unaffected by this exposure.

Due to the pervasiveness of environmental pollution in bee habitats, I exposed bumble bees to cadmium, copper, selenate, imidacloprid, and hydrogen peroxide and found that each of these compounds can be lethal to bees. I also showed that most of these chemicals can affect the diversity of the bee microbiome and that there is interstrain variation in toxicant tolerance genes in the major bee symbionts Snodgrassella alvi and Gilliamella apicola.

As exposure to cadmium or selenate has been shown to affect animal-associated microbes, I assayed the effects of these chemicals on honey bees and observed shifts in the bee microbiome at multiple timepoints. I also found that exposure to selenate and cadmium changes the overall bee metabolome and may cause oxidative damage to proteins and lipids. Lastly, I found that bee-associated bacteria can bioaccumulate cadmium but generally not selenate.

In this dissertation I demonstrated that bee-associated bacteria are generally robust to toxicant exposure, but that chemicals can alter the composition of both bumble bee and honey bee microbiomes. I also show that toxicants affect bee metabolism, and that the bee microbiome plays an important role in maintaining host health when challenged with toxicants.

The honey bee, Apis mellifera, pollinates a wide variety of essential crops in numerous ecosystems around the world but faces many modern challenges. Among these, the microsporidian pathogen Nosema ceranae is one of the primary detriments to honey bee health. Nosema infects the honey bee gut, which harbors a highly specific, coevolved microbiota heavily involved in bee immune function and nutrition. Here, we extend previous work investigating interactions between the honey bee gut microbiome and N. ceranae by studying experimentally infected bees that were returned to their colonies and sampled 5, 10, and 21 days post-infection. We measured Nosema load with quantitative PCR and characterized microbiota with 16S rRNA gene amplicon sequencing. We found significant colony level variation in infection levels, and subtle differences between the microbiota of colonies with high infection levels versus those with low infection levels. Two exact sequence variants of Gilliamella, a core gut symbiont that has previously been associated with gut dysbiosis, were significantly more abundant in bees from colonies with high Nosema loads versus those with low Nosema loads. These bacteria deserve further study to determine if they facilitate more intense infection by Nosema ceranae.